Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Presenting as Recurrent and Migrating Focal Cortical Encephalitis

Xiang, Xinran; Evans, Rachel L; Lovera, Jesús; Rao, Rashmi

doi:10.1177/2329048x20966172

Cited by 4 publications

(1 citation statement)

References 15 publications

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“…29 The presence of such follicles strongly correlates with disability progression and disease severity. 40 It is worth noting that recently also MOG-associated diseases [63][64][65] and, very rarely, neuromyelitis optica spectrum disorders have been reported in association with meningitis. 66…”

Section: Pia Mater Arachnoidea and The Dura-arachnoidea Barriermentioning

confidence: 99%

Characterization of immune responses in the meninges

Merlini¹

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Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS), which is characterized by plaque-like demyelination in both white and grey matter and diffuse neurodegeneration. A T cell-driven autoimmune response against CNS antigens is the initiating event in the MS pathogenesis, as demonstrated in the animal model of MS, experimental autoimmune encephalomyelitis (EAE). In EAE, CNS-reactive T cells reach the CNS through pial vessels and accumulate in the leptomeninges, from where they invade the CNS parenchyma. Also in human MS, the leptomeninges were shown to be a site of inflammation, and their involvement correlates with disease severity.The role of the leptomeninges as a crucial checkpoint for the initiation of the disease has been therefore well documented. On the other hand, it remains unknown whether the outer meningeal layers, i.e. the dura mater, can contribute to the development of neuro-inflammation in EAE and be a site for T-cell trafficking to and from the CNS. Moreover, it has not been investigated whether CNS-invading T cells can also possibly leave the CNS via the dura.Recent studies proposed that the dura might represent an exit route for cells and solutes from the CNS, which could travel to the deep cervical lymph nodes via the dura lymphatics.

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Section: Pia Mater Arachnoidea and The Dura-arachnoidea Barriermentioning

confidence: 99%

Characterization of immune responses in the meninges

Merlini¹

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Electroclinical features of seizures in myelin oligodendrocyte glycoprotein antibody-associated cerebral cortical encephalitis: A case report and literature review

Tokumoto

Nishida

Kawaguchi

et al. 2022

Seizure

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Leptomeningeal Enhancement in Multiple Sclerosis and Other Neurological Diseases: A Systematic Review and Meta-Analysis

Ineichen

Tsagkas

Absinta

et al. 2021

Preprint

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BackgroundThe lack of systematic evidence on leptomeningeal enhancement (LME) on MRI in neurological diseases, including multiple sclerosis (MS), hampers its interpretation in clinical routine and research settings.PurposeTo perform a systematic review and meta-analysis of MRI LME in MS and other neurological diseases.Materials and MethodsIn a comprehensive literature search in Medline, Scopus, and Embase, out of 2292 publications, 459 records assessing LME in neurological diseases were eligible for qualitative synthesis. Of these, 135 were included in a random-effects model meta-analysis with subgroup analyses for MS.ResultsOf eligible publications, 161 investigated LME in neoplastic neurological (n=2392), 91 in neuroinfectious (n=1890), and 75 in primary neuroinflammatory diseases (n=4038). The LME-proportions for these disease classes were 0.47 [95%-CI: 0.37–0.57], 0.59 [95%-CI: 0.47–0.69], and 0.26 [95%-CI: 0.20–0.35], respectively. In a subgroup analysis comprising 1605 MS cases, LME proportion was 0.30 [95%-CI 0.21–0.42] with lower proportions in relapsing-remitting (0.19 [95%-CI 0.13–0.27]) compared to progressive MS (0.39 [95%-CI 0.30–0.49], p=0.002) and higher proportions in studies imaging at 7T (0.79 [95%-CI 0.64–0.89]) compared to lower field strengths (0.21 [95%-CI 0.15–0.29], p<0.001). LME in MS was associated with longer disease duration (mean difference 2.2 years [95%-CI 0.2–4.2], p=0.03), higher Expanded Disability Status Scale (mean difference 0.6 points [95%-CI 0.2–1.0], p=0.006), higher T1 (mean difference 1.6ml [95%-CI 0.1–3.0], p=0.04) and T2 lesion load (mean difference 5.9ml [95%-CI 3.2–8.6], p<0.001), and lower cortical volume (mean difference −21.3ml [95%-CI −34.7–-7.9], p=0.002).ConclusionsOur study provides high-grade evidence for the substantial presence of LME in MS and a comprehensive panel of other neurological diseases. Our data could facilitate differential diagnosis of LME in clinical settings. Additionally, our meta-analysis corroborates that LME is associated with key clinical and imaging features of MS.PROSPERO No: CRD42021235026.Summary statementOur systematic review and meta-analysis synthesize leptomeningeal enhancement proportions across a comprehensive panel of neurological diseases, including multiple sclerosis, and assesses its prognostic value in multiple sclerosis.Summary dataLeptomeningeal enhancement (LME) is a nonspecific imaging feature present across many neurological disorders, including neoplasm, infection, and primary neuroinflammation.The presence of LME is associated with worse clinical and imaging outcomes in multiple sclerosis, justifying its ascertainment in clinical practice.Neuroinflammatory animal models can be used to further investigate the pathophysiology of LME, including its pathological tissue signature and/or its association with cortical pathology.

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Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Presenting as Recurrent and Migrating Focal Cortical Encephalitis

Cited by 4 publications

References 15 publications

Characterization of immune responses in the meninges

Characterization of immune responses in the meninges

Electroclinical features of seizures in myelin oligodendrocyte glycoprotein antibody-associated cerebral cortical encephalitis: A case report and literature review

Leptomeningeal Enhancement in Multiple Sclerosis and Other Neurological Diseases: A Systematic Review and Meta-Analysis

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